The Journal of Trauma and Acute Care Surgery最新文献

Background: Venous thromboembolism (VTE) remains a frequent postinjury complication with well established but nonmodifiable risk factors. We hypothesized that fibrinolysis shutdown (SD) as measured by thromboelastography (TEG) would be an independent risk factor for VTE in trauma patients.

Methods: A subgroup of patients enrolled in the CLOTT-2 (Consortium of Leaders in the Study of Traumatic Thromboembolism 2), multicenter prospective cohort study had kaolin TEG and tissue plasminogen activator (tPA)-TEG data at 12 and 24 hours postadmission. Patients underwent a screening duplex venous ultrasound examination during the first week unless clot was already detected on computed tomography. Injury factors associated with early fibrinolysis SD (defined as kaolin TEG Ly30 ≤0.3%) and/or tPA resistance (tPA-R) (defined as kaolin TEG with tPA 75 ng Ly30 <2.1%) were investigated as was the association of the TEG measurements with the development of VTE.

Results: A total of 141 patients had both TEG measurements at 24 hours, and 135 had both TEG measurements at 12 hours. Shutdown was evident at 12 hours in 71 of 135 (52.6%) patients and in 62 of 141 (44%) at 24 hours. Tissue plasminogen activator resistance was found in 61 of 135 (45.2%) at 12 hours and in 49 of 141 (34.3%) at 24 hours. Factors significantly associated with SD included receiving >4 U of FFP in the first 24 hours, the presence of a major brain injury or pelvic fracture, and the need for major surgery. In contrast, factors significantly associated with early tPA-R included >4 U of red blood cells transfused in the first 24 hours and the presence of a major chest injury or long bone fracture. Deep vein thrombosis was detected in 15 patients and pulmonary clots in 5 (overall VTE rate, 14.2%). Tissue plasminogen activator resistance at 12 hours was found to be an independent risk factor for VTE (hazard ratio, 5.57; 95% confidence interval, 1.39-22.39).

Conclusion: Early development of a hypercoagulable state as defined by tPA-R at 12 hours after admission represents a potentially modifiable risk factor for postinjury VTE.

Level of evidence: Therapeutic/Care Management; Level II.

Background: MG53, a member of the tripartite motif (TRIM) protein family, plays an essential role in cell membrane repair and promotes cell survival. Recent studies show that systemic delivery of recombinant human MG53 (rhMG53) protein markedly attenuates tissue injury/inflammation, and facilitates healing. This study was performed to test whether intravenous administration of rhMG53 protein would decrease the lesion size in a clinically relevant large animal model of traumatic brain injury (TBI).

Method: Yorkshire swine (40-45 kg; n = 5/group) were subjected to controlled cortical impact TBI and randomized to either: (1) rhMG53 protein (2 mg/kg, intravenous) or (2) normal saline control. Hemodynamics, intracranial pressure, and brain oxygenation were monitored for 7 hours. Brains were then harvested and sectioned into 5-mm slices and stained with 2,3,5-triphenyltetrazolium chloride to quantify the lesion size. Blood-brain barrier permeability of MG53 in the brain was determined by Western blot and immunohistochemistry. Bcl-2 and phospho-GSK β levels were measured as makers of prosurvival pathway activation.

Results: Hemodynamic parameters were similar in both groups, but the lesion size in the rhMG53-treated group (2,517 ± 525.4 mm 3 ) was significantly ( p < 0.05) smaller than the control group (3,646 ± 740.1 mm 3 ). In the treated animals, rhMG53 was detected in the regions surrounding the TBI, but it was absent in the saline-treated control animals. Bcl-2 and phospho-GSK β levels in the brains were upregulated in the rhMG53-treated animals.

Conclusion: Intravenously administered rhMG53 localizes to the injured areas of the brain, with the treated animals demonstrating a significant attenuation in the brain lesion size following TBI.

Abstract: "Scoop and run" approaches for severely injured patients have been adopted by emergency medical services over the past 40 years. This has resulted in more patients with severe injuries including penetrating cardiac wounds arriving at trauma centers and other acute care hospitals. General surgery trauma teams and general surgeons taking trauma call are the first responders for diagnosis, resuscitation, and operative management of injured patients. By natural selection, 96% to 98% of patients with signs of life on arrival to the trauma center after sustaining a penetrating cardiac wound have injuries that are amenable to repair by a general surgeon, fellow, or senior surgical resident without the need for a cardiothoracic surgeon or cardiopulmonary bypass.This literature and experience-based review summarizes the diagnostic and operative approaches that should be known by all trauma teams and general surgeons taking trauma call. In addition, it describes when a cardiothoracic surgeon should be consulted and briefly reviews how complex penetrating cardiac injuries are repaired.